Efecto perjudicial de la pandemia por SARS-CoV-2 en la sintomatología digestiva en pacientes con síndrome de intestino irritable / Detrimental impact of SARS-CoV-2 pandemic in the symptomatology of patients with irritable bowel syndrome

Irritable Bowel Syndrome (IBS) is a more frequent disorder in the brain-gut axis interaction in the world. COVID-19 has affected the population's mental health, and its impact on clinical severity in patients with IBS is unknown. Objective: To evaluate the effect of psychosocial stress produced by the pandemic on the severity of gastrointestinal symptoms. Methodology: 54 women and three men with IBS were interviewed by telephone. Factors associated with quality of life, comorbidities, IBS subtype, and COVID-19 diagnosis were asked. Calls were developed between June 2020 to January 2021. Results: 75% had Diarrheal IBS (IBS-D), 67% had comorbidities, 47% with busy work, and 70% in person, five patients (9%) were diagnosed with COVID-19. Of the total, 88% referred to change in gastrointestinal symptoms, 56% increased abdominal pain, and 95% bloating. Abdominal pain was negatively associated with quality of life (p < 0.036), and the incomplete evacuation's sensation positively with difficulty sleeping (p < 0.034). Conclusion: In this study, IBS patients interviewed by telephone reported higher abdominal pain and subjective bloating associated with the pandemic by SARS-CoV-2. Keywords: Irritable

El Síndrome de Intestino Irritable (SII) es uno de los trastornos en la interacción cerebrointestino más frecuentes en el mundo. La pandemia COVID-19 ha afectado la salud mental de la población, siendo desconocido su impacto en la severidad clínica en pacientes con SII. Objetivo: Evaluar el efecto del estrés psicosocial producido por la pandemia en la severidad de síntomas gastrointestinales de pacientes con SII. Metodología: 54 mujeres y 3 hombres con SII fueron entrevistados vía telefónica. Se preguntó por factores asociados a calidad de vida, comorbilidades, subtipo de SII y diagnóstico de COVID-19. Las llamadas se realizaron entre junio de 2020 hasta enero de 2021. Resultados: Un 75% presentó SII Diarreico (SII-D), el 67% comorbilidades, el 47% con trabajo activo y 70% presencial, 5 pacientes (9%) diagnosticados COVID-19. Del total, 88% refirió cambio en síntomas gastrointestinales, 56% aumentó el dolor abdominal y 95% la distensión abdominal. El dolor abdominal se asoció negativamente con la calidad de vida (p < 0,036), y la sensación de evacuación incompleta positivamente con la dificultad para dormir (p < 0,034). Conclusión: En este estudio, los pacientes con SII entrevistados vía telefónica reportaron mayor dolor y distensión abdominal subjetiva asociado a la pandemia por SARS-CoV-2.

Las alteraciones de la microbiota intestinal en la patogenia del hígado graso no alcohólico / Alterations of the intestinal microbiota in the pathogenesis of nonalcoholic fatty liver disease

Non-alcoholic fatty liver disease (NAFLD) is currently considered in Chile and worldwide, as the main cause of cirrhosis and liver transplantation. It is therefore one of the main public health objectives for reducing its prevalence. In last years, it was suggested that the intestinal microbiota (IM) might contribute to the pathophysiology of NAFLD, as well as in the progression toward nonalcoholic steatohepatitis (NASH) and cirrhosis. It is known that changes in the composition of IM are associated with alterations in intestinal permeability and the production of inflammatory metabolites. These alterations are part of the pathophysiological mechanisms leading to the development of NASH. However studies on MI in patients with NAFLD and NASH in Chile are scarce. Through a research grant, recently awarded at the Hospital Clínico Universidad de Chile, we aim to confirm and characterize the intestinal dysbiosis associated with NAFLD in Chilean patients and to establish the relationship between the changes in microbial composition with the progression of liver damage. The description of these alterations represents an opportunity to explore new therapeutic approaches for future interventions. In effect, through the restoration of an intestinal microbial environment towards homeostasis in these patients, we expect to reverse or improve the progression of damage provoked by this disease. (AU)

Influencia del polimorfismo genético rs2927488 de Bcl3 en el síndrome de intestino irritable / Influence of genetic polymorphism rs2927488 of the Bcl3 irritable bowel syndrome

Irritable Bowel Syndrome (IBS) is a functional disorder characterized by abdominal discomfort associated with changes in bowel habit and increased intestinal sensitivity. It is one of the most common disorders of digestive health in Chile as well as in the world. Although the pathophysiological mechanisms of IBS have yet to be fully established, it is known that (epi-) genetic factors are involved in the development of the disorder. Bcl3 (B-cell leukemia/lymphoma 3) is a regulatory protein of the intestinal inflammatory response, specifically, with regard to the signaling pathways of NF-kB (Nuclear Factor-kB). Among the variability of the human genome, the gene encoding Bcl3 contains the polymorphism SNPs rs2927488 (variants A/G) which has been associated with susceptibility to developing Inflammatory Bowel Disease (IBD). Furthermore, the presence of this polymorphic variant has been correlated with increased levels of Bcl3 gene expression in patients with Crohn’s Disease. Our laboratory is focused on understanding the potential relationship between Bcl3 and IBS. Our preliminary studies describe an increased expression of Bcl3 at the intestinal mucosal epithelium in IBS patients with a diarrheal-phenotype (IBS-D). We are now interested to investigate if the presence of the variant SNP rs2927488(A/G) is a susceptibility factor for IBS development and to understand the significance of its relationship with Bcl3 expression, in Chilean IBS patients. In this review, we focus primarily on the relationship between rs2927488(A/G) polymorphism of Bcl3 gene, its protein expression and its mechanisms of control over the inflammatory response...

Síndrome de intestino irritable, un proceso inflamatorio de bajo grado: ¿mito o realidad? / IBS, a low grade inflammatory process: myth or reality?

Irritable bowel syndrome (IBS) is one of the most prevalent functional disorders in Chile impacting on socio-economic development due to significantly impaired quality of life of the individual. It is characterised by abdominal discomfort associated with alterations in bowel habit and increased visceral hypersensitivity. One of the outstanding features of IBS is the presence of a bi-directional imbalance of gut-brain interactions, which can induce alterations in the intestinal immune response. IBS is characterised by increased intestinal mast cell activity associated with alterations of para-cellular permeability and activation of sensory nerve endings. The increased proximity of mast cell to colonic nerves is correlated with abdominal pain and increased visceral hypersensitivity of the patients. In spite of the well-described role of mast cell in the induction of mucosal inflammation, in IBS only a low-grade inflammation is observed. The present review discuses the possible immune-regulatory mechanisms that are involved in IBS pathophysiology.

El síndrome de intestino irritable (SII) es considerado uno de los trastornos funcionales más prevalente en Chile, que impacta el desarrollo socio-económico del país debido al deterioro de la calidad de vida de los individuos que lo portan. Es caracterizado por molestias abdominales asociadas a alteraciones en el hábito de defecación e hipersensibilidad visceral. Una de las características más destacadas en el SII es la presencia de un desequilibrio de las interacciones en el eje intestino-cerebro, el cual puede inducir alteraciones en la respuesta inmune intestinal. El SII es caracterizado por una aumentada actividad de los mastocitos en el intestino, asociada con alteraciones en la permeabilidad para-celular epitelial y la activación de terminaciones nerviosas en la mucosa intestinal. El aumento de la cercanía de los mastocitos a nervios colónicos está relacionado con el dolor abdominal y la hipersensibilidad visceral de los pacientes. Pese a que está muy bien descrito el papel del mastocito en la inducción de la inflamación en mucosas, en el SII se observa sólo un bajo-grado de inflamación. En la presente revisión se discute los posibles mecanismos regulatorios inmunes que están involucrados en la fisiopatología del SII.

Mycobacterium avium subsp paratuberculosis y enfermedad de Crohn: evidencias de una zoonosis / Possible association between Mycobacterium avium subsp paratuberculosis infection and Crohn's disease

Paratuberculosis is a chronic intestinal disease of animals caused by Mycobacte-rium avium subsp. paratuberculosis (MAP), which has some pathological features similar to Crohn's disease (CD) in humans. The presence of MAP in food for human consumption and in affected tissues of patients with CD has been detected. Therefore, a causal association between this microorganism and the disease in humans, has been postulated. However, several related studies have failed to confirm this hypothesis and the scientific acceptance of MAP as a zoonotic agent remains controversial. This review presents the main findings related to this issue, contrasting evidences for and against an association between MAP and CD. The need to promote national studies focusing on this area is suggested.

Papel del sistema inmune en el desarrollo de las enfermedades inflamatorias intestinales / Role of the immune system in inflammatory bowel diseases development

Las enfermedades inflamatorias intestinales (EII), entre las que se incluyen a la enfermedad de Crohn (EC) y colitis ulcerosa (CU), son patologías de etiología multifactorial, en las cuales se ha demostrado en los últimos años que el componente genético tiene un papel relevante. La incidencia de estas patologías ha ido en aumento en los países desarrollados y también en Chile. A pesar de los avances en su estudio, la etiología de las EII no está totalmente esclarecida, aunque es posible reconocer factores genéticos, inmunológicos y ambientales en su patogénesis. Entre los posibles mecanismos propuestos la respuesta alterada a antígenos bacterianos cumpliría un papel relevante en un subgrupo de pacientes con EC quienes presentan alguna mutación en los receptores que reconocen patógenos. Esta revisión analiza avances recientes en el conocimiento de las EII y destaca los hallazgos relacionados con alteraciones en los componentes del sistema inmune gastrointestinal y su posible relación con la patogenia de las EII. Un análisis detallado de la interrelación entre los diferentes integrantes del sistema inmune de la mucosa intestinal, tales como las células dendríticas, epiteliales, de Paneth y los linfocitos T y su actividad defectuosa podría brindar nuevas herramientas para el diseño de estrategias experimentales y terapéuticas de las EII.